OBJECTIVE The authors present a case of recovery of saccular function after vestibular rehabilitation. MATERIAL AND METHOD Vestibular rehabilitation is proposed to a patient presenting a left lateral body deviation as well as postural disorders at the time of the vertical movements and in car, associated with an unilateral abolition of vestibular evoked myogenic potentials (VEMP). RESULTS We observe a recovery of VEMP and a disappearance of symptomatology after vestibular rehabilitation. CONCLUSION A loss of saccular function can involve a postural disorder in some circumstances. The best treatment is vestibular rehabilitation. We insist on the need for knowing otolithic semiology in order to propose suitable explorations and therapy.

La méthode de training autogène de Schultz (TA) est une technique de relaxation par entraînement à l’autohypnose. Dans ce travail nous l’appliquons à des patients qui présentent une pathologie vertigineuse chronique apparue au décours d’une atteinte lésionnelle vestibulaire. Une angoisse plus ou moins importante accompagne toujours les plaintes fonctionnelles de ces patients. Cette angoisse est efficacement prise en charge par le TA qui implique un travail centré sur le corps. Cette méthode peut par ailleurs faciliter dans un deuxième temps une approche psychothérapique classique.

On four occasions since 1978, this 53 year-old woman presented with a right hemicorporal hypotonia, symptomatic of a hemispheric cerebellar syndrome. In 1981, she experienced the progressive development of a cervical dystonia. CT scan and RM scan showed a cavernous angioma in the right cerebellar hemisphere. The 18F-2-fluoro-2-deoxy-glucose PET scan revealed a right cerebellar and a controlateral cortical and striatal hypometabolism. This crossed cerebello-cortical diaschisis can be interpreted as a functional interruption of the cerebello-cerebral pathways. This case raises the question of the role played by a cerebellar lesion in the development of a focal dystonia.

Magnetic resonance imaging (MRI) was performed in 20 patients with multiple sclerosis and abnormal electro-oculographic examination. All but 2 patients showed MRI abnormalities in the infratentorial region: hypersignal on T2-weighted sequences and/or images of atrophy. Usually, each patient had multiple abnormalities, which could prevent anatomico-oculographic correlations. With oculomotor disorders of cerebellar origin, correlations between clinical findings and MRI images were satisfactory, but with disorders due to brainstem lesions correlations were not so good, as shown by the results in 9 patients with internuclear ophthalmoplegia.

In a clinicotopographic study of 14 patients with internuclear ophthalmoplegia (INO) confirmed by electrooculography (EOG), the pattern of visual dysfunction was compared to the location and severity of lesions of the medial longitudinal fasciculus (MLF) visualized by magnetic resonance imaging (MRI). Of the 12 patients with classically-defined 'anterior' INO, nine were classed as having definite multiple sclerosis (MS), and three as probable or possible. Five of the 12 had MR-imaged MLF lesions, and five including one with MLF lesions, had cerebellum-associated lesions. Of the two patients with so-called 'posterior' INO, one presented a heredodegenerative disease and cerebellum-related lesions, and in the other, a non-visual neurological condition was not diagnosed. The finding that MR-imaged MLF lesions do not always occur simultaneously with INO may indicate that INO could be the expression of a functional disorder in the posterior fossa, preceding MLF lesion development.

Two cases of spontaneously regressing encephalitis with ataxia during Epstein-Barr virus infectious mononucleosis in two previously healthy young adults are described. Apart from the signs of cerebellar lesions, electrooculography revealed nystagmic bursts changing direction every 3 to 4 seconds, overlying slow oscillations of the eyes, which the authors propose calling 'short-period alternating nystagmus'.

Recordings of ocular movements during reading in hemianopic patients showed an increase in global reading time related mainly to the increase in number of movements of progression and regression in left hemianopsia and to the time to return to the line in right hemianopsia. Comparison of these changes with those noted in the same patients during recordings of elementary ocular movements and reading simulation suggests that they are not only of a linguistic and/or cognitive type but that they may also be related to altered sensorial data such as size of words or place of spaces between words.

This chapter discusses a study involving the reading of eye movements of homonymous hemianopia patients. The study explained in the chapter analyzes the qualitative and/or quantitative changes of the oculomotor scanning behavior in reading when visual information is available only in one hemifield as it is for hemianopic readers. The study involves reading eye movements of the control group in accordance with the classical staircase pattern and hemianopic group. According to the organization of patients' reading eye movements, three main types of changes are defined. The chapter explains how a right visual defect disturbs reading eye movement more than a left eye defect. The impairment of saccadic movements is not correlated with neuropsychological findings, as hemineglect and the disturbance of reading eye movements in LHH are caused by the oculomotor disturbance itself rather than spatial agnosia.

A study of the oculomotor scanning behaviour and the reading per­ formances of eight left-brain damaged patients with right homonymous hemianopia, as compared with 10 normal readers, revealed two groups of patients. The first group (6 Ss) they kept the same staircase pattern in the successive saccadic movements and the reading eye movements as was observed in the control group. The only changes consisted of an increased number of shorter saccades. Their mean reading time was in­ creased but these patients were able to read without paralexic errors. In the second group (2 Ss), the successive saccadic movements to the right side were dysmetric, but the staircase pattern was still recognizable in the saccadic movements to the left. Their oculomotor behaviour in reading was completely disorganized and their reading abilities were impaired. A possible adaptation of reading oculomotor behaviour to a right visual defect is demonstrated. It depends on a preserved saccadic movements to the right side. The disturbance of the right saccadic movements itself prevents the adaptation and impairs the different reading processes.

Etude electronystagmographique de 85 sujets de 75 a 86 ans souffrant de vertiges. 75% d'ENG du type deficitaire dont 25% de syndromes vestibulaires peripheriques, 40% de syndromes vestibulaires centraux et 10% d'hyporeflectivite vestibulaire

The behavior of 64 normal subjects was studied after they had been submitted to excentric lateral ocular fixation of gaze of more than 40 degrees for periods of one the three minutes. A significant proportion developed vertigo, slow segmental deviations and nystagmus. Nystagmus appearing during gaze fixation (physiological nystagmus of extreme lateral gaze) was distinguished from nystagmus in the opposite direction which appeared after cessation of fixation and was named "post-fixation nystagmus". The possible role of proprioceptive receptors in the extra-ocular muscles is discussed and a hypothesis proposed of an oculo-oculogyric reflex possibly through the vestibular nuclei and influencing the control mechanisms of posture and balance.

A similar affection has developed in eight members from four generations of a family living in the Alsace. The disease is characterized by the onset of a pyramidal, pseudobulbar syndrome and dementia during the third or fourth decade of life. The outcome is fatal after a mean period of three years. Cerebral biopsies in three cases have demonstrated multicentric amyloid plaques differing from senile plaques. Clinical and pathological findings are similar to those currently reported in the literature as being typical of Gerstmann-Sträussler-Scheinker's syndrome. The affection appears as a separate entity: the multicentric plaques, clinical symptomatology, pyramidal or pseudobulbar, cerebellar syndromes, usually preceding dementia, age of onset, course, and familial character or the disorder distinguish it among presenile dementias. Its clinical profile and course are very similar to that of familial cases of Alzheimer's disease, some of which are probably cases of Gerstmann-Strässler-Scheinker's syndrome. Transmission to animals, though inconstant, places it within the group of transmissible dementias among kuru, Creutzfeldt-Jakob's, and familial forms of Alzheimer's disease. The familial nature of the affection and the variability of clinical and pathological features in the same family illustrate the complex relationships between hosts and pathogenic agents in the clinicopathological expression of a disease.